End-Tidal CO2 Pressure and Cardiac Performance during Exercise in Heart Failure


Medicine & Science in Sports & Exercise: January 2009 - Volume 41 - Issue 1 - pp 18-24
doi: 10.1249/MSS.0b013e318184c945
Clinical Sciences

Introduction: In patients with heart failure (HF), end-tidal CO2 pressure (PetCO2) is related to ventricular function at rest and has been shown to predict prognosis. However, little is known about the association between ventricular performance and PetCO2 responses to exercise.

Methods: Forty-eight patients with HF and 13 normal subjects underwent cardiopulmonary exercise testing (CPX), while cardiac output and other hemodynamic measurements at rest and during exercise were obtained using a novel, noninvasive, bioreactance device based on assessment of relative phase shifts of electric currents injected across the thorax, heart rate, and ventricular ejection time. CPX responses and indices of cardiac performance were compared between normal subjects and HF patients achieving above and below a PetCO2 of 36 mm Hg at the ventilatory threshold (PetCO2@VT).

Results: HF patients with an abnormal PetCO2@VT (<36 mm Hg) had a lower exercise capacity, a lower V˙O2@VT, a higher V˙E/V˙CO2 slope, and lower oxygen uptake efficiency slope (OUES) values compared with normal subjects and patients achieving a normal PetCO2@VT. Patients with reduced PetCO2@VT had lower peak cardiac output responses to exercise (20.0 ± 10, 17.8 ± 6, and 13.7 ± 7 L·min−1 for normal subjects and HF patients with normal and abnormal PetCO2 responses to exercise, respectively, P = 0.04). PetCO2@VT was inversely related to the V˙E/V˙CO2 slope (r = −0.78, P < 0.001) and directly related to the OUES (r = 0.55, P < 0.001).

Conclusion: Reduced PetCO2 reflects impairments in the functional, ventilatory, and cardiac performance response to exercise in patients with HF. PetCO2 can supplement other clinical and CPX indices in the functional and prognostic evaluation of patients with HF.

1Cardiology Division, Veterans Affairs Palo Alto Health Care System, Stanford University, Palo Alto, CA; 2Texas Tech University of Health Sciences, Amarillo, TX; 3Lonestar Arrhythmia and Heart Failure Center, Amarillo, TX; 4Albert Einstein College of Medicine/Montefiore Medical Center, Bronx, NY; and 5Columbia University, New York, NY

Address for correspondence: Jonathan Myers, Ph.D., Cardiology Division-111C, Veterans Affairs Palo Alto Health Care System, 3801 Miranda Ave, Palo Alto, CA 94304; E-mail: drj993@aol.com.

Submitted for publication May 2008.

Accepted for publication June 2008.

© 2009 American College of Sports Medicine